Emodin / cycE/CCNE Cancer Research Results

EMD, Emodin: Click to Expand ⟱
Features:
Organic compound isolated from rhubarb, buckthorn, knotweed. It has laxative, anticancer, antibacterial, antiinflammatory, and antiviral activities, and is used in traditional Chinese medicine.
Emodin, an anthraquinone derivative found in various plants (e.g., rhubarb, Polygonum cuspidatum).

Pathways:
- Generation of Reactive Oxygen Species (ROS)
- Upregulation Bax downregulation of Bcl‑2, caspase activation and cyt_c release.
- Induce cell cycle arrest at various checkpoints (commonly G0/G1 or G2/M phases.
- Can inhibit NF‑κB activation
– MAPK Pathways
– PI3K/Akt Pathway
- Metalloproteinases (MMPs)

-ic50 cancer cells 10-50uM, normal cells higher(supports a therapeutic window)

Rank Pathway / Target Axis Direction Label Primary Effect Notes / Cancer Relevance Ref
1 Reactive oxygen species (ROS) ↑ ROS Driver Upstream cytotoxic trigger Emodin induces ROS in cancer cells; ROS increase is positioned upstream of mitochondrial dysfunction and death signaling. (ref)
2 Mitochondrial integrity (ΔΨm) ↓ ΔΨm Driver Mitochondrial dysfunction Emodin decreases mitochondrial membrane potential (ΔΨm), consistent with mitochondria-dependent killing. (ref)
3 Intrinsic apoptosis (caspase cascade) ↑ apoptosis (↑ caspases / ↑ PARP cleavage) Driver Execution-phase cell death Emodin activates caspase-dependent apoptosis with mitochondrial involvement in colon cancer models. (ref)
4 AMPK → AKT/mTOR axis ↑ AMPK / ↓ AKT-mTOR signaling Secondary Growth/metabolic suppression NSCLC study reports AMPK activation with inhibition of AKT/mTOR alongside apoptosis and ROS increase (consistent directionality). (ref)
5 NF-κB signaling ↓ NF-κB activation (↓ p65 nuclear translocation; ↓ IκBα phosphorylation/degradation) Secondary Reduced pro-survival/inflammatory transcription Emodin inhibits TNF-α–induced NF-κB activation by blocking IκBα phosphorylation/degradation and p65 nuclear activity. (ref)
6 STAT3 signaling ↓ STAT3 activation (↓ phosphorylation) Secondary Reduced survival/proliferation signaling HCC study shows emodin suppresses STAT3 activation (and discusses upstream kinase modulation), supporting directionality as STAT3↓. (ref)
7 HIF-1α hypoxia program ↓ HIF-1α (↓ biosynthesis; not via transcription/stability) Adaptive Reduced hypoxia tolerance Pancreatic cancer study: emodin decreases HIF-1α by decreasing biosynthesis (explicit mechanism stated). (ref)
8 Aerobic glycolysis (Warburg output) ↓ glycolysis (↓ ECAR / ↓ glycolytic dependence) Phenotypic Metabolic suppression Renal cancer paper reports emodin inhibits aerobic glycolysis (and links killing to a non-apoptotic death mode in that model). (ref)
9 HDAC inhibition (epigenetic enzyme activity) ↓ HDAC activity Secondary Epigenetic modulation Direct biochemical evidence: emodin inhibits HDAC activity in vitro (fast-on/slow-off kinetics reported). (ref)
10 NRF2 / HO-1 antioxidant response ↑ NRF2 / ↑ HO-1 (context-dependent stress response) Adaptive Counter-response to redox stress HCC model reports emodin increases NRF2 and HO-1 expression; interpret as adaptive/compensatory (not necessarily the cytotoxic driver). (ref)


cycE/CCNE, Cyclin E: Click to Expand ⟱
Source:
Type:
Cyclin E regulates multiple downstream molecules, such as the retinoblastoma susceptibility gene (RB1) and the transcription factor E2F.
Cyclin E (Cyclin E1 and Cyclin E2) is the key regulator of the late G1 → S-phase transition.
Cyclin E is a prognostic marker in breast cancer, its altered expression increased with the increasing stage and grade of the tumor.
Cyclin E is a regulatory protein that plays a critical role in the cell cycle, particularly in the transition from the G1 phase to the S phase. Its expression levels can significantly influence cancer progression and patient prognosis.

Cyclin E expression is frequently elevated in various cancers and is generally associated with poor prognosis. Its role in promoting cell cycle progression makes it a potential biomarker for tumor aggressiveness and patient outcomes.


Scientific Papers found: Click to Expand⟱
1332- EMD,    Induction of Apoptosis in HepaRG Cell Line by Aloe-Emodin through Generation of Reactive Oxygen Species and the Mitochondrial Pathway
- in-vivo, Nor, HepaRG
*tumCV↓, *ROS↑, *MMP↓, *Fas↑, *P53↑, *P21↑, *Bax:Bcl2↑, *Casp3↑, *Casp8↑, *Casp9↑, *cl‑PARP↑, *TumCCA↑, *P21↑, *cycE/CCNE↑, *cycA1/CCNA1↓, *CDK2↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Bax:Bcl2↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Fas↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   cycA1/CCNA1↓, 1,   cycE/CCNE↑, 1,   P21↑, 2,   TumCCA↑, 1,  
Total Targets: 15

Scientific Paper Hit Count for: cycE/CCNE, Cyclin E
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:75  Target#:378  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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